The rod cells of vertebrate retinas are responsible for vision at low levels of light. The visual pigment, rhodopsin, absorbs light as the primary event. This is followed by a series of events which leads to hyperpolarization of the plasma membrane of the rod outer segment and results in a nerve impulse. This proposal deals with the molecular mechanisms involving rhodopsin function and the phospholipid matrix which are important in early events of visual transduction. The stability of the disk lipid bilayer will be investigated after specific modifications of the lipid matrix both in the presence and absence of rhodopsin. These modifications include changes in lipid composition, Ca2+ concentrations, and pH. The effect these modifications exert on rhodopsin will also be investigated with respect to the protein stability and function. The rhodopsin molecule will be subjected to modifications at specific sites. The effect of these modifications will be investigated with respect to rhodopsin function and membrane stability to identify more specifically how rhodopsin functions in visual transduction. The stabilization of the disk bilayers with respect to the role of both protein (rhodopsin and opsin) and phospholipid composition should be of value in understanding membrane degenerative diseases such as retinitis pigmentosa. The role of himicholinium-containing phospholipids in experimentally induced retinal degeneration will be directly addressed. The role of cholesterol in modulating rhodopsin function will be determined.